作者: Anthony Chalmers , Peter Johnston , Mick Woodcock , Michael Joiner , Brian Marples
DOI: 10.1016/J.IJROBP.2003.09.053
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摘要: Abstract Purpose Poly(ADP-ribose) polymerase-1 (PARP-1) is rapidly and directly activated by single-strand breaks required for efficient base excision repair. These properties indicate that inhibition of PARP-1 might enhance the cellular response to low doses radiation. We tested effect chemical on low-dose clonogenic survival in a number cell lines radiation knockout murine line. Methods materials Clonogenic V79-379A CHO-K1 hamster fibroblasts, T98G U373-MG human glioma cells, 3T3 mouse embryo fibroblast cells was measured using precise flow cytometry-based plating assay. Chemical inhibitors PARP enzymes were their after range ionizing doses. Results activity induced marked radiosensitization V79, CHO, exponentially growing 0.05–0.3-Gy range. This not seen U373 or confluent populations. Low-dose apparent cells. Conclusion actively dividing tumor suggests they may have role enhancing efficacy ultrafractionated low-dose-rate radiotherapy regimens. hypothesize PARP-2 compensates absence